primary infantile glaucoma
Introduction
Introduction to primary infantile glaucoma Primary infantile glaucoma (primaryinfantileglaucoma) is a congenital hereditary trabecular meshwork or iris corneal keratosis that hinders the discharge of aqueous humor and forms neonatal and infant glaucoma. The disease is a hereditary disease. More men than women. Mostly, the incidence of both eyes is about 25-30%. About 80% of the symptoms and signs appear within 1 year of age, and the rest are shown at 1-6 years old. Its main manifestations are photophobia, tearing, eyelids, corneal enlargement, edema, turbidity, rupture of the posterior elastic layer, and elevated intraocular pressure. The disease is not sensitive to drug treatment, mainly surgical treatment. If early diagnosis and early surgical treatment are available, about 80% of patients can control intraocular pressure. basic knowledge The proportion of illness: 0.0021% Susceptible population: newborn, infant, male than female Mode of infection: non-infectious Complications: keratitis
Cause
Primary infantile glaucoma cause
Congenital factors (95%):
Although it is generally believed that the mechanism of elevated intraocular pressure in primary infantile glaucoma is due to congenital factors leading to abnormal development of the iris cornea angle, which leads to obstruction of aqueous outflow, but so far, the iris corneal keratosis development, abnormal differentiation, The precise process of trabecular dysplasia and how to produce such abnormalities and other pathological and pathological mechanisms is still not fully understood. There are still many controversial issues. In fact, the formation of the iris cornea angle, the differentiation of the anterior horn network and Schlemm The appearance of the tube has undergone a very complicated process of biological development, and any problem in any one of the links may cause a poor outflow of aqueous humor.
Pathogenesis
Regarding the theory of the pathogenesis of primary congenital glaucoma, although it has been generally accepted that the abnormal development of iridocorneal angle causes obstruction of aqueous outflow is the idea of elevated intraocular pressure in primary congenital glaucoma, but due to the normal angle The precise process of development, differentiation, division, and specialization is not fully understood. Therefore, there are various different theories about the exact pathogenesis for a long time. The more representative theories are summarized as follows:
1.Barkan Membrane Theory Barkan first proposed in 1955 that primary congenital glaucoma occurs because the cells in the mesoderm are incompletely reabsorbed during the development of the embryo, leaving a layer of impervious film covering the surface of the corner. It hinders the outflow of aqueous humor and leads to an increase in intraocular pressure. Later, it was observed by scanning electron microscopy that the trabecular meshwork has a continuous endothelial layer. Under normal circumstances, the fetus forms a cavity-like cavity in the last few weeks of development. Primary congenital glaucoma remains as a non-permeable membrane, so they support the theory that the presence of Barkan membrane is the cause of primary congenital glaucoma. The operation of angle incision for congenital glaucoma is Designed according to this theory.
At present, there is a different view on the theory of Barkan membrane, because it can not fully explain all the phenomena, some examinations have not found the existence of the membrane, in addition, some primary congenital glaucoma has poor curative effect on the angle of the incision, so Barkan's membrane theory may not be the only mechanism of primary congenital glaucoma.
2. Immature atrophy of the iris corneal angle is not complete Mann believes that primary congenital glaucoma is due to incomplete atrophy of the mesoderm atrophy of the iris cornea, which hinders the outflow of aqueous humor and causes an increase in intraocular pressure.
3. The mesoderm division of the iris cornea is incomplete Allen, Burian, Braley et al. pointed out that the mesoderm division of the iris cornea angle does not completely cause the congenital defect of the angle.
4. Iliac corneal trabecular tissue cell rearrangement failure Smalser and Ozanics explain the pathogenesis of primary congenital glaucoma. During the early re-alignment of the iris keratocytes, the mesoderm incorrectly enters the normal small The beam net, which affects the outflow of aqueous humor, and subsequent examination by light microscopy and electron microscopy revealed changes in the structure of uveal trabeculae in primary congenital glaucoma and in the endothelial cells of Schlemm tubes in some infants and young glaucoma patients. A thick layer of amorphous material also supports this view.
5. The development of neural crest cells is blocked. Johnston's research shows that the interstitial layer of the cornea, the endothelium, the iris, the ciliary body, the sclera, the trabecular meshwork and the uveal lining are all derived from neural crest cells, once they originate from neural crest cells. The iris corneal angle is blocked and its structure changes abnormally.
6. Comprehensive theory Because none of the above single theories can fully explain the pathogenesis of primary congenital glaucoma, a comprehensive theory has been proposed: primary congenital glaucoma occurs from neural crest cells. The development of the iris corneal angle is blocked, and the outflow of aqueous humor is blocked by one or more mechanisms; the high position of the ciliary body and the iris is attached to the trabecular meshwork, resulting in compression of the mesh of the trabecular meshwork; Different plane developmental abnormalities, such as Schlemm's tube anomalies, may also be the cause.
In conclusion, there are still different perspectives on the pathogenesis of primary congenital glaucoma so far, and the exact cause will be further studied.
Prevention
Primary infantile glaucoma prevention
Pay attention to pregnancy care, prevent viral infections, and patients with family history pay attention to prenatal diagnosis.
Complication
Primary infantile glaucoma complications Complications keratitis
Secondary glaucoma with other dysplasia, such as Axenfeld-Rieger syndrome, Sturge-Weber syndrome and maternal rubelle syndrome, can be found, most of the causes of this abnormality and congenital infant glaucoma It is fundamentally different, and the angle of the incision for the treatment of primary infantile glaucoma, the external trabeculectomy is very poor, occasionally trabecular dysgenesis and other dysplasia coexist It can be explained by the damaged tissue for the same neural crest cell source. Some diseases such as glaucoma combined with Sturge-Weber syndrome have the same iris angle in histology as the primary infantile glaucoma. On the etiology of glaucoma, Increased scleral venous pressure may be an additional cause. The iris corneal angle of maternal rubella syndrome is clinically and histopathologically similar to primary infantile glaucoma. Some reports on primary infantile glaucoma, actual The parental rubella syndrome is not obvious or the clinical symptoms are not obvious.
Symptom
Primary infantile glaucoma symptoms Common symptoms High intraocular pressure tears keratitis myopia astigmatism
1. Photophobia, tearing, and eyelids are the three most characteristic symptoms of this disease. When these symptoms appear in newborns or infants, they should be further examined.
2, the cornea is enlarged, the anterior chamber is deepened, and the transverse diameter of the cornea exceeds 12 mm (the normal corneal transverse diameter generally does not exceed 10.5 mm). Due to elevated intraocular pressure, the corneal epithelium often has edema, and the appearance is frosted or dull. Sometimes the posterior elastic membrane is ruptured, typically as a stripe turbidity in the deep horizontal or concentric circles of the cornea. Prolonged damage can result in varying degrees of corneal opacity.
3, elevated intraocular pressure, abnormal angle of the corner, glaucoma optic disc depression and increased axial length of these signs are important for the diagnosis of congenital glaucoma, but often need to be examined under general anesthesia, in order to fully confirm. With the exception of chloralkanones, most general anesthetics and sedatives have a lowering of intraocular pressure. Therefore, in the evaluation of infants' intraocular pressure measurements, anesthetic and sedative factors should be considered. For some infants under 6 months, breastfeeding or Illness is measured after breastfeeding, and intraocular pressure measurement can also be performed under epidemax.
4, characteristic deep anterior chamber disease often has, the angle of the corner may be found in the anterior position of the iris insertion, the anterior chamber crypt is missing, the surrounding iris pigment epithelium masks the angle of the anterior chamber, or thickened uveal trabecular meshwork.
5, the normal disc of the optic disc is pink, the physiological cup is small and the eyes are symmetrical. The childhood glaucoma cup is progressive, vertical or concentric, and after the intraocular pressure control, some large cups cannot be reversed.
6. Ultrasound measurement and follow-up of the length of the axial length of the eye can help to determine whether there is progress in glaucoma in infants and young children.
Examine
Examination of primary infantile glaucoma
1. Histopathological examination:
It was found that the angle of the anterior chamber of the primary infantile glaucoma was changed before the iris was attached, the iris was present, and the sclera was not developed. The longitudinal fibers of the ciliary muscle were directly attached to the trabecular meshwork, and the trabecular mesh was thick and thin, varying in length. The "trabecular bundles" that make up the trabecular meshwork are abnormally thickened, closely arranged or fused together, the trabecular plate is compressed, the mesh is narrowed, and there are deposits such as proteins and cell debris, broken organelles and denatured in the trabecular meshwork. There are different degrees of fibrosis in the protein deposits. The Schlemm tube is fissure or linear stenosis. The surface is covered with primitive mesenchymal tissue. There is an amorphous substance under the endothelium of the Schlemm tube area. The endothelial cells are degenerated and necrotic, and the organelles are sparse. Increased ribosomes, expansion or dissolution of the endoplasmic reticulum, formation of vacuoles in the cytoplasm and formation of a large number of microfilaments, mitochondrial swelling, most of which did not show a non-permeable membrane, but saw the compact formed by the trabeculae under the light microscope Can not be distinguished as a single cell or a thin plate, giving the illusion of a continuous membrane, the trabecular plate is in tension, especially when the peripheral iris retreats, due to abnormalities of the longitudinal fibers of the ciliary muscle In the trabeculae, when the muscles contract, the trabecular plate is tight, and the trabecular space is closed, resulting in an increase in the outflow resistance of the aqueous humor. It is found that the red blood cells can pass through the inner trabecular space, and in the compressed lateral trabecular space and adjacent No red blood cells were seen in the Schlemm tube area, indicating that the lesion occurred in this part.
2. Corneal examination
Including corneal diameter, degree of edema turbidity and rupture of the elastic layer.
(1) Corneal diameter: Usually measured by caliper (or compass) for corneal transverse diameter, the result is recorded in mm, accurate to 0.5, normal corneal transverse diameter is 10 ~ 10.5mm, increased by 0.5 in the first year after birth ~1.0mm, the corneal diameter exceeding 12.0mm in the first year after birth should be highly suspected as infantile glaucoma.
(2) corneal edema opacity: early cases due to epithelial and epithelial edema, mild pale milky corneal opacity, if the parenchyma also edema, opacity is very obvious, acute corneal edema seen in the corneal rupture of the eye The cornea becomes grayish white, like the corneal appearance of mild chemical injury. In the long-term, severe corneal edema will cause permanent scarring, which will increase the opacity of the cornea, and will not restore transparency even if the intraocular pressure is controlled.
(3) rupture of the posterior corneal elastic layer: Observe whether there is Haab pattern in the deep part of the cornea of the eye. The performance of different parts has its own characteristics: the central area of the near cornea is horizontal line, and the peripheral part is curved or parallel with the limbus.
3. Intraocular pressure measurement
The intraocular pressure of primary infantile glaucoma is generally 30 ~ 50mmHg, but also up to 80mmHg or more. As with the diagnosis and treatment evaluation of primary open angle glaucoma, the intraocular pressure value is important and necessary, but not the primary infant. The only diagnostic and therapeutic evaluation index for infantile glaucoma, intraocular pressure imaging is of little value in the diagnosis of such glaucoma, and the factors affecting intraocular pressure measurement are many, such as the depth of anesthesia in infants and young children, the measured tonometer and technique, and the large lesions. Eyeballs, etc.
(1) The effect of general anesthesia: related to the degree of anesthesia and the role of the drug itself, the intraocular pressure can be increased during the anesthesia period, and the intraocular pressure can be lowered during the deep anesthesia period, and all anesthetics can affect the intraocular pressure. However, the degree of conventional examination of infantile glaucoma is mostly based on ketamine basic anesthesia, and has an analgesic effect, generally do not require pre-anesthesia medication, ketamine intramuscular injection 4 ~ 8mg / kg After the injection, it will take effect within 10 minutes. The effect only lasts for about 30 minutes. After waking, you can continue to sleep for several hours. Ketamine has the effect of excitatory sympathetic nerves, which can increase blood pressure and increase heart rate, thus making the intraocular pressure mild. Elevated, but no clinically significant changes in intraocular pressure have been found in the application. In recent years, there has also been a rapid onset (about 30 s), short-acting intravenous general anesthetic propofol (2,6-diisopropyl) Pediatric anesthesia for children, intravenous anesthesia induction in children > 8 years old requires about 2.5mg / kg, lower than this age requires more drugs, through continuous infusion or repeated single injection can maintain the requirements of anesthesia Depth, usually 9 to 15 mg / (kg · h) The rate of administration or the amount of 25 mg (2.5 ml) to 50 mg (5.0 ml) per administration can achieve satisfactory anesthesia. No propofol is currently found to have an effect on intraocular pressure, but the drug has no analgesic effect, check or Local anesthetics are required for surgery.
(2) tonometer and measurement method: tonometer itself can cause measurement error of intraocular pressure, Schiötz tonometer can measure eye pressure due to corneal edema, corneal surface deformation and curvature change and ball wall hardness, etc. The influence of factors, hand-held applanation tonometer avoids the error caused by the hardness of the eye wall of infants and young children, but the radius of curvature of the cornea caused by the change of eye structure is flat, the opacity of the cornea, etc., also requires fluorescein, Tono-pen eye The pressure gauge (pen type) has a small measuring head area (only 1.5mm in diameter) and is in contact with the cornea with a sterile disposable latex sleeve to avoid microbial infection of the eye. The operation is simple and convenient, and is not affected by the overall morphology and curvature of the cornea. It is the ideal method for measuring intraocular pressure of infantile glaucoma. Because of the increase of eyeball in the eye, no matter which kind of tonometer is used to measure intraocular pressure, care should be taken to avoid the impact of eyelids. Do not oppress the eyeball when opening the eyelid. Use a spring opener or eyelid pull hook to gently lift the help to open the file.
(3) The influence of large eyeballs on the lesion: The change of anatomical structure of the affected eye has two effects on the measurement of intraocular pressure. First, the eyeball is enlarged to make the contents of the eyelids full, and the eyelids are tight. If the intraocular pressure is measured, it is not noticed. To the effect of the eyelids, the measured intraocular pressure is often high. Second, the increase of the eyeball makes the wall of the ball thinner, the curvature of the cornea becomes flat, and the corneal edema often makes the measured intraocular pressure low.
4. Anterior chamber and iris corneal angle
The cornea and corneoscleral margin of the affected eye are more obvious, and the anterior chamber is generally deep. The purpose of the iris corneal angle is mainly to find evidence for determining the primary or secondary type of glaucoma. As long as the cornea is not obvious edema and opacity. It should be carried out directly under the operating microscope to view the angle of the eye of the eye with a Goldman corner mirror. It is convenient and easy to perform. Typical primary glaucoma angles of the infants and young children are covered with thick brown bands covering the entire trabeculae. The area of the iris to the surrounding iris, the width of the root of the iris is different. Microscopic magnification shows that the dark brown band is the cord-like mesophyll tissue, which is called the iris or comb ligament in the clinic. Sparse hairy, some areas densely rooted, distributed forward over the scleral process and trabecular mesh, no brown band corners, no trabecular mesh structure, dense, unstructured area The band is directly connected to the attachment of the iris root. Inexperienced doctors often mistake these changes for pre-irisal adhesions, milder primary glaucoma, and their angles develop. Some areas may be better, normal or near normal trabecular meshwork structures can be seen, and the corner regions of normal and developmental disorders in the same eye can alternate between different quadrants.
5. Fundus examination
Mainly to observe whether there is glaucomatous change in the optic disc, the optic disc depression of primary infant glaucoma has its characteristics: the enlarged cup concave is located in the center of the optic disc, which is both round and deep, which is closely related to the development of infant eyeballs. There are 200 cases in China. The characteristics of neonatal optic disc morphology were studied. It was found that the frequency distribution of normal newborn cup-to-plate ratio (C/D) was significantly skewed, and the C/D value was small. The number of discs in the 400 eyes was 31.25%. ; C / D 0.3 accounted for 95.75%; > 0.3 accounted for 4.25%; 0.6 only 0.05%, two eyes C / D equal 74.5%, the difference 0.1 97%, indicating two eyes in normal newborns C/D is basically consistent. It has been reported in foreign countries that C/D>0.3 is 2.7% (26/936) in normal children, 0.6% (3/468) in both eyes, and C/D in glaucoma. For those with greater than 0.3, 61% (52/85), single eye glaucoma patients with 89% (24/27) of the optic disc cup asymmetry, the above data indicate that C/D greater than 0.3 is not a pathological standard, but within 1 year The child should be highly suspicious, and the asymmetry of the two-eye disc cup also has a large diagnostic reference value.
6. Ultrasound biomicroscopy
In the 1990s, ultrasound biomicroscopy (UBM) was applied to the clinic. UBM can be used to detect the characteristics of the anterior segment of the ocular anterior segment in vivo. It is a non-invasive, painless study of the ultrasound diagnosis of the anterior segment of the eye. In the new method, 11 eyes of 6 infants with glaucoma were examined by UBM, and the anatomical features and anterior segment structure were evaluated. UBM can treat the iris cornea, iris, lens, ciliary body and anterior chamber angle. The images were displayed in detail. In the eyes of 8 trabecular mesh-deficient eyes, all of them had elongate and advanced ciliary processes, no abnormalities in the trabecular meshwork and anterior chamber, and 3 eyes with thick opacity in the cornea. The severe structure of the anterior segment of the eye is destroyed and the cornea of the central region is thinned, and the posterior pole of the cornea is depressed. This indicates that UBM is used to evaluate the structure of congenital infant glaucoma with corneal opacity. The results of the examination can be helpful for the decision of treatment. There are authors in China who use UBM to measure and dynamically visualize the anterior segment structure of 38 cases (58 eyes) of primary infant glaucoma with a 50MHz UHF ultrasound probe. Examination, the results of the child, regardless of the onset of disease, severity or age, the most important lesion is the relative position of the scleral process and the apex of the angle of the apex, 3 / 4 of the eye sclera is located outside the apex of the corner or after Externally, the scleral process of the 1/4 eye is parallel to the attachment of the iris. The length and thickness of the ciliary process are larger than those of normal children of the same age. The ciliary process is forward and inward, and some of them are attached to the iris. Changes in the relative position of the scleral process and the apex of the anterior chamber in patients with primary infantile glaucoma suggest a pathological basis for scleral dysplasia or iris attachment.
Diagnosis
Diagnosis and diagnosis of primary infantile glaucoma
diagnosis
Primary infantile glaucoma presents typical manifestations, such as corneal enlargement, opacity, Haab pattern, elevated intraocular pressure, enlarged cup of the optic disc, etc., which is easy to make a diagnosis, but these cases have more or less visual function. Direct damage, and indirect damage caused by changes in the anatomical structure of the eyeball indirectly affect the visual function of the function. Therefore, early diagnosis is necessary, according to the observation of the parents' relatives, the clinical manifestations of the child and the detailed Ophthalmologic examination makes a comprehensive judgment. There are many children with primary infantile glaucoma in the clinic because of photophobia, tearing, corneal edema and opacity, and corneal inflammation. In infants, there are photophobia, tears, and eyelids. Eyeball and corneal enlargement, etc., should be alert to the possibility of glaucoma, and the following examination: Most cases under the general anesthesia under a comprehensive examination, based on the above performance characteristics is not difficult to make a correct diagnosis, such as The measured intraocular pressure is normal, but the clinical signs of other infantile glaucoma exist, and can also be diagnosed as primary infantile glaucoma, intraocular pressure In the normal range, the measured intraocular pressure may be affected by the multiple factors mentioned above. Hoskins et al. measured a group of normal infants (74 eyes) and primary infant glaucoma (159 eyes) under general anesthesia. The results of intraocular pressure are: normal infants and young children have 12% 21mmHg, while primary infantile glaucoma 21mmHg accounted for 91%, if the lack of corneal enlargement and optic disc cup is not obvious, even if the intraocular pressure is high, temporarily No diagnosis, when the above examination is not clear, parents should be told to closely observe the symptoms of the child, regular follow-up, can be reviewed after 4 to 6 weeks, observe changes in the cornea, intraocular pressure and fundus to obtain more diagnostic support evidence.
Differential diagnosis
There are several common eye diseases that need to be differentiated from primary infantile glaucoma, mainly because some of the symptoms or manifestations of these diseases are similar to those of primary infantile glaucoma, but there is no fear of light, tears, or eyelids. , corneal enlargement and Haab pattern, all the characteristics of the expansion of the optic disc cup, other important medical history including family history (especially siblings), history of maternal infection (rubella) during pregnancy and birth history (whether or not the birth control), suspected glaucoma and Identification of other diseases is very useful.
1. Large cornea (magalocornea) is a rare congenital anomaly, the incidence of both eyes, 90% found in men, attribute-linked recessive inheritance, corneal transparency, diameter often 14 ~ 16mm, large cornea can be associated with deep anterior chamber, iris tremor and Abnormal diopter, normal angle of the anterior chamber or trabecular pigmentation, but also obvious iris protrusion, but the large cornea has no posterior elastic layer rupture, increased intraocular pressure and enlarged optic disc cup and other primary infantile glaucoma signs, visual function No damage, it is reported that some patients in some families have large corneas and others have glaucoma, so some people think that it is a different phenotype of genetic diseases related to primary infantile glaucoma. Clinically, it is clinically For any large corneal cases, follow-up should be strengthened, paying special attention to the presence or absence of intraocular pressure and optic disc changes. The large cornea may also be enlarged due to the anterior segment of the eye, the lens suspensory ligament is fragile and fractured, and subluxation occurs, resulting in secondary glaucoma. The characteristics of the large cornea itself and its corresponding performance are not difficult to distinguish from the primary infantile glaucoma.
2. Corneal cramps and laboratories can cause damage to the neonatal eyeballs when the birth control is difficult to produce, which can cause corneal edema. The posterior elastic layer rupture is often multiple, showing vertical or oblique stripes. The level of primary infantile glaucoma or the rupture of the posterior elastic layer concentric with the limbus, the corneal forceps injury is often monocular, the left eye is more than the right eye, because the fetus at birth is mostly the left anterior position. Corresponding eyelid skin and tissue around the eyelid often have signs of trauma at the same time. The rupture of the posterior corneal layer can exist for life. The corneal edema can last for 1 month or more, but the cornea does not enlarge, the intraocular pressure is normal or low, and the optic disc is normal. Characteristic performance and history of forceps assisted delivery, easy to identify with glaucoma.
3. Congenital hereditary corneal endothelial dystrophy is an autosomal recessive hereditary disease at birth. The clinical manifestations are photophobia, tearing and decreased vision. It is characterized by corneal edema in both eyes, but the cornea is normal and no intraocular pressure. Increased, corneal haze-like edema at the beginning, the parenchyma layer is ground-glass opacity, the center of the cornea is heavier, gradually expanding to the periphery, and finally the whole cornea is extremely diffusely thickened, and the cornea may have band-like degeneration, scars and new blood vessels. The corneal endothelial cells are significantly reduced or lacking.
4. Lacrimal duct obstruction may have tears, but fearless light, usually seen in neonatal lacrimal duct hypoplasia, in the normal development of the eye, the lower end of the tear duct has a half-moon valve called Hasner flap, valve function, tear overflow Newborns often cause obstruction due to the residual membrane at the lower end of the nasolacrimal duct. The eyeballs are normal. If neonatal dacryocystitis occurs, it is often accompanied by mucopurulent secretions. When the cornea is involved, there may be photophobia and eyelids, but the cornea is absent. Enlargement, compression of the lacrimal sac often has more purulent secretions. If necessary, it can be examined under general anesthesia and rinsed in the lacrimal passage, or even explored to confirm the presence or absence of lacrimal passage obstruction.
5. High myopia and primary infantile glaucoma are easily confused with its large eyeball performance, especially in monocular patients, lack of photophobia, tearing, eyelids, corneal enlargement and Haab pattern, the fundus entrance is tilted, the surrounding With the characteristics of pathological myopia such as scleral ring (myopia arc) and choroidal atrophy, the axial length of the eye is obviously increased. With the increase of age, the myopia and the axial length can be gradually increased, but the intraocular pressure is normal.
6. Optic pits are a type of developmental abnormality on the optic disc, which is characterized by a clear circular or elliptical depression on the upper edge of the optic disc, mostly on the temporal side (about 3/4), on the central optic disc, often Occasionally, it is found in the fundus examination that the congenital small concave is mostly single eye, the diameter of the optic disc is 1/6 to 1/3, the depth is 2 to 7D, and the majority is 1. The wall of the congenital concave is steep and colored. Gray or yellow, with nerve fibers, blood vessels and glial tissue at the edges, patients have no symptoms, but visual field examination can be expressed in various forms of visual field defects. The difference from primary infantile glaucoma lies in the congenital depression of the optic disc. It is static, and there is no corneal enlargement, edema turbidity and elevated intraocular pressure.
7. Optic disc physiological large vision cup is also a kind of developmental abnormality of optic disc, which is thought to be caused by excessive atrophy of the original epithelial papilla (Bergmeister papilla) during embryonic development. Except for the large depression of the optic cup, it is not associated with other glaucoma. The clinical manifestations, physiological large cups have been reported in the population C / D 0.5 accounted for 6%, may have family tendencies, in the same family, there may be several or several generations of members with similarly shaped optic disc According to the investigation of the physiologic large-vision cup family, the occurrence of physiological large-vision cup is related to heredity, which may be autosomal dominant inheritance. The physiology of the large-vision cup is normal, the cup is uniform, and there is no retinal optic nerve. Any damage, as normal function, has no characteristic clinical manifestations of primary infantile glaucoma.
